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Biologie der Epidermodysplasia-verruciformis-assoziierten HPV

Biology of epidermodysplasia verruciformis-associated HPV

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Zusammenfassung

Das Genus β-Papillomvirus (βPV) umfasst gegenwärtig mehr als 40 Virustypen einschließlich der sog. Epidermodysplasia-verruciformis (EV)-assoziierten HPV, die ursprünglich mittels Southern-Blot-Hybridisierung bei EV-Patienten nachgewiesen wurden. βPV sind in der Allgemeinbevölkerung ubiquitär verbreitet und etablieren sich oft schon in den ersten Lebenswochen. Haarfollikel gelten als natürliches Reservoir. Etwa 25% der bei Erwachsenen nachgewiesenen βPV persistieren über mindestens 9 Monate. Aufgrund sehr geringer Virusproduktion erfolgt die Serokonversion gegen βPV nur schleppend. Keratinozytenhyperproliferation bei Psoriasispatienten oder nach schweren Verbrennungen stimuliert die Virusreplikation. Massive Virusreplikation ist nur bei EV-Patienten zu beobachten, verbunden mit der Induktion disseminierter Hautläsionen mit einem hohen Risiko für maligne Entartung. Bei 75% der EV-Patienten ist dies auf homozygote inaktivierende Mutationen in den Genen EVER1 oder EVER2 zurückzuführen. Ein transgenes Mausmodell belegte die kritische Bedeutung einer durch UV-Bestrahlung oder Verwundung stimulierten HPV8-Onkogenexpression für die Tumorinduktion.

Abstract

The genus betapapillomavirus (betaPV) presently comprises more than 40 virus types including the so-called epidermodysplasia verruciformis (EV)-associated HPV, which were originally detected in EV-patients by Southern blot hybridization. BetaPV are ubiquitous in the general population and frequently establish themselves already during the first weeks of life. Hair follicles are regarded as natural reservoir. About 25% of betaPV detected in adults persist for at least 9 months. Due to very low virus production, seroconversion against betaPV starts sluggishly. Hyperproliferation of keratinocytes in psoriasis patients or after severe burns stimulates virus replication. Massive virus replication only occurs in EV-patients, associated with the induction of disseminated skin lesions with a high risk of malignant conversion. In 75% of EV-patients this can be put down to homozygous, inactivating mutations in the genes EVER1 or EVER2. A transgenic mouse model substantiated the crucial role of increased HPV8 oncogene expression, induced by UV-irradiation or wounding, for tumor induction.

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  1. Institut für Virologie, Nationales Referenzzentrum für Papillom- und Polyomaviren, Fürst-Pückler-Str. 56, 50935, Köln, Deutschland

    H. Pfister

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Pfister, H. Biologie der Epidermodysplasia-verruciformis-assoziierten HPV. Hautarzt 62, 17–21 (2011). https://doi.org/10.1007/s00105-010-2030-8

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